Along with the vascular lesions characteristic of diabetic retinopathy, considerable clinical evidence exists that the retinal pigment epithelium (RPE) is affected in diabetic eye disease. Biochemical and physiological studies of animal models suggest that diabetic pigment epitheliopathy may be a complication mediated by the activity of the enzyme aldose reductase. We are utilizing cultured human and monkey RPE as an in vitro model system to study the effects of elevated hexoses on these cells. In common with other tissues in the presence of high sugar concentrations, transport of the amino acid taurine into cultured RPE cells incubated with galactose is impaired. In addition, the galactose- treated cells are "leakier" in such a way as to actually extrude taurine. Both of these effects can be partially prevented by incubation with aldose reductase inhibitor (ARI) supplemental to the galactose. Since taurine is essential for normal retinal function, a deficit in RPE handling of taurine under diabetic conditions may contribute to retinal pathology.